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At least 55 records · Page 3Linked to original sources
PubMed1994

Malnutrition and gastrointestinal dysfunction as prognostic factors for survival in familial amyloidotic polyneuropathy.

OBJECTIVES: To describe the evolution of nutritional and neurological complications in a Swedish population of patients with familial amyloidotic polyneuropathy, and to identify prognostic factors and useful tests for monitoring the progress of the disease. DESIGN: Prospective and retrospective study of patients with familial amyloidotic polyneuropathy. SETTING: Tertiary referral centre. SUBJECTS: Twenty-seven patients with familial amyloidotic polyneuropathy, and a symptomatic onset before the age of 50. MAIN OUTCOME MEASURES: Age at onset, duration of disease before death, serum albumin, body mass index (BMI), duration and grade of peripheral neuropathy and gastrointestinal disturbances. Faecal fat, xylose test and 75selenohomocholic acid-taurine (SeHCAT) test were used for assessment of malabsorption. RESULTS: Thirteen patients died during the study period after a disease duration of between 9 and 18 years (mean 13). A short time interval between the onset of neurological and of gastrointestinal symptoms had greater impact on survival than age at onset in this selected group of patients (r = 0.65; P = 0.017). Malnutrition was evaluated by multiplying the [body weight (kg)/height2 (m)] with the serum albumin to compensate for oedema. This modified body mass index (mBMI) was significantly correlated to the number of years before death (r = 0.89; P < 0.0005) and to the duration of gastrointestinal symptoms (r = -0.66; P < 0.0005), but not to duration of disease (r = -0.2; P = 0.20). Polyneuropathy was graded according to functional capacity from I to IV (PND score) and was correlated to the number of years before death and mBMI, but not to serum albumin. The SeHCAT test for bile acid malabsorption was significantly correlated to the duration of gastrointestinal symptoms and to mBMI (r = -0.67; P = 0.0003 and r = -0.62; P = 0.003, respectively). CONCLUSION: The investigation disclosed that a short time interval between the onset of neurological and of gastrointestinal symptoms is associated with a decreased survival time. The mBMI was closely related to time before death, duration of gastrointestinal disturbances, malabsorption and functional capacity. The mBMI appears to be well suited to monitoring disease progress and gives prognostic information.

Adult↗
PubMed1987

Gastrointestinal dysfunction among intensive care unit patients.

This study used the Acute Physiological and Chronic Health Evaluation (APACHE II) system to select two groups of ICU patients with comparable risk of hospital death to evaluate the importance of GI dysfunction, defined as failure to tolerate enteral nutrition (EN), as a prognostic factor. In our ICU, patients who have not undergone recent bowel surgery are treated by EN. Those patients who cannot tolerate EN are treated by total parenteral nutrition (TPN). One hundred and eleven patients who tolerated EN (functioning gut) and 97 TPN patients who failed to tolerate EN (GI dysfunction) were studied. The mean APACHE II scores of the two groups were 17.7 +/- 6.5 (SD) and 17.7 +/- 5.1, respectively. The observed mortality of patients with GI dysfunction (51%) was significantly higher (p less than .0005) than that of patients with a functioning gut (25%). This was associated with significantly poorer APACHE II mean BP, oxygenation, and creatinine scores among the GI dysfunction patients. Our results suggest that shock, ischemia, and hypoxemia, in addition to causing impairment of renal function, may bring about changes in the GI tract, evident clinically only as a failure to tolerate EN, which have an adverse effect on the prognosis of ICU patients so affected.

Adult↗
PubMed1989

Gastrointestinal dysfunction and its effects on nutrition in CF.

Prevention of malnutrition, a consequence of elevated energy requirements, increased losses and low caloric intake, is one of the main goals in the treatment of cystic fibrosis. Caloric stool losses, catch-up growth and an elevated energy expenditure, even in the absence of overt lung disease and malabsorption, have led to recommendations for a caloric intake of 120-150% of the recommended daily allowances. A high energy intake with a fat content of at least 40 calorie % and adequate pancreatic supplementation has shown to improve growth and median age of survival. As a rational treatment of the fundamental disturbance in cystic fibrosis, a decrease in chloride permeability across epithelia, is not yet available, treatment should be concentrated on adequate nutritional support in combination with optimal correction of those gastrointestinal abnormalities including faecal bile acid loss, small intestinal abnormalities, pancreatic insufficiency, hormonal abnormalities and disturbances in gastrointestinal motility, which may aggravate maldigestion and malabsorption.

Cystic Fibrosis↗
PubMed2000

Neurologic and gastrointestinal dysfunction in cardio-facio-cutaneous syndrome: identification of a severe phenotype.

Controversy exists over the distinction between cardio-facio-cutaneous (CFC) syndrome and Noonan syndrome (NS). Several authors have suggested that they are different phenotypes of the same condition. We present the cases of two patients with CFC syndrome to show that it is a distinct condition with a unique combination of findings and a more complex natural history. These patients, both girls, were born with signs of fetal edema following pregnancies complicated by polyhydramnios. Each has short stature with relative macrocephaly; fuzzy, sparse hair; and the typical craniofacial features, including a square forehead. Both have heart abnormalities, failure to thrive, and severe feeding problems requiring gastrostomy. They are markedly hypotonic and developmentally delayed. They show signs of frequent eyelid fluttering and have oral aversion, tactile hypersensitivity, and sensory integration abnormalities. Keratosis pilaris, the characteristic skin symptom, is also present in both patients. In a review we identified 56 cases of CFC syndrome. We scored these cases by 10 clinical criteria and identified a subset with a specific, severe phenotype distinct from that of NS. The serious neurologic and gastrointestinal complications, in addition to the skin abnormalities and characteristic facies in this group, clearly separate these patients from the mildly affected ones, most of whom appear to have NS or another syndrome. We discuss the differences between the severe CFC phenotype and those of overlapping conditions. We set forth stringent diagnostic criteria for CFC syndrome, the initial step toward identifying a molecular basis for this condition.

Child, Preschool↗
PubMed1998

Role of motility measurements in managing upper gastrointestinal dysfunction.

Nausea, vomiting, and abdominal pain are common symptoms that suggest many diagnoses. The patient's symptoms may be related to an anatomical defect such as a peptic ulcer or a mechanical small bowel obstruction. However, no anatomical abnormality may be identified despite radiological, endoscopic, or laboratory studies. The cause of the patient's symptoms may have significant impact on the patient's quality of life (nonulcer dyspepsia) and life span (intestinal pseudo-obstruction). Abnormal antroduodenal motility may be the underlying cause of the patient's symptoms. Normally, coordinated phasic contractions in the stomach and small intestine maintain digestion and absorption of food. A prolonged set of phasic contractions (phase 3 of the migrating complex) begins in the stomach and propagates down the small intestine to excrete nondigestible foods, bacteria, and dead cells. Any disturbance in the normal motility pattern can lead to maldigestion and symptoms of upper intestinal dysfunction. Objective tests of motility disturbances in the stomach and small intestine include measurement of gastric emptying, intestinal transit, contractions of the stomach and duodenum, and electrogastrography. Abnormal antroduodenal motility may be secondary to an abnormality in the smooth muscle (myopathy) or the nerves in controlling smooth muscle contractions (neuropathy). Antroduodenal motility measurements may help identify a partial small bowel obstruction, the cause of small intestinal overgrowth, and the cause of chronic abdominal visceral pain. Motility studies may suggest useful drugs for correcting the underlying pathophysiology and relieving symptoms.

Gastrointestinal Diseases↗
PubMed1994

Ophthalmoplegia, demyelinating neuropathy, leukoencephalopathy, myopathy, and gastrointestinal dysfunction with multiple deletions of mitochondrial DNA: a mitochondrial multisystem disorder in search of a name.

This article describes a 37-year-old woman with progressive external ophthalmoplegia, peripheral neuropathy, and chronic intractable diarrhea. Laboratory studies disclosed lactic acidosis, ragged red fibers lacking cytochrome c oxidase, high-normal muscular mitochondrial enzymes, demyelinating neuropathy, leukoencephalopathy and multiple mitochondrial DNA deletions. This is the fourth patient described with this clinical syndrome, which represents a separate entity among multisystemic mitochondrial disorders. The patient described here is the first with this syndrome to have multiple mitochondrial DNA deletions.

Adult↗
PubMed1985

Gastrointestinal dysfunction in the critically ill: nutritional implications.

Parenteral therapy is frequently indicated for initial repletion in the severely malnourished patient. Attention should be paid to the nutrients required for initial repletion based on the patient's metabolic needs at the time of therapy, as well as allowance for adequate calories for repletion of body and muscle mass. After the initiation of parenteral therapy and the adequate replacement of fluids and electrolytes, slow introduction of oral or enteric feeding is reasonable. This probably is best handled initially by the use of a nasogastric or nasoenteric feeding tube. However, if the patient willingly ingests oral feedings, the oral route is certainly favorable. Close attention should be paid to the adequacy of gastric emptying. Symptoms of abdominal bloating and diarrhea may require modification of the rate at which oral intake is progressing.

Colitis, Ulcerative↗
PubMed1986

Home parenteral nutrition for patients with advanced intraperitoneal cancers and gastrointestinal dysfunction.

The use of total parenteral nutrition (TPN) in patients with advanced, untreatable cancer is controversial. Occasionally, however, damage to bowel by tumor, radiation, or surgery renders these patients unable to eat and TPN may be indicated to prevent premature death from starvation. We have used Home Parenteral Nutrition (HPN) to support three patients with advanced, untreatable abdominal cancer and inability to eat. Morbidity was minimal and survival times were 24, 6 and 1.5 months. Payment was covered by third party agencies. All patients and their families were gratified by the ability to return home with nutritional support. HPN can be used to support terminal cancer patients with bowel obstruction and may afford them longer survival. Ideally, patients considered for this should be well motivated, with good support systems, and with survival estimated to be at least months.

Abdominal Neoplasms↗
PubMed1994

Primary acute simian immunodeficiency virus infection of intestinal lymphoid tissue is associated with gastrointestinal dysfunction.

Human immunodeficiency virus (HIV)-associated intestinal abnormalities can occur before immunodeficiency or infection with opportunistic enteropathogens. Rhesus macaques infected with simian immunodeficiency virus (SIV) develop an AIDS-like illness that frequently includes enteropathy. The development of enteropathy and its association with SIV infection in the intestinal tract was examined. By 1 week after infection, SIV-infected macrophages and T lymphocytes were detected in gut-associated lymphoid tissue. In contrast to findings in the asymptomatic stage, SIV-infected macrophages were numerous in primary and terminal stages of infection. An acute enteropathy syndrome was observed in the primary acute stage of infection. Functional abnormalities of absorptive epithelium, indicated by D-xylose malabsorption and decreased sucrase activity, occurred before the onset of diarrhea or opportunistic enteric infections. These findings indicate that macrophages and T cells in the intestinal tract are early targets of SIV infection and may play a critical role in the development of SIV-associated intestinal dysfunction.

Acute Disease↗
PubMed1996

The role of nitric oxide in ethanol-induced gastrointestinal dysfunction.

We recently showed that acute ethanol inhibits contractility of the lower esophageal sphincter (LES) and the lower esophageal body (LEB) both in vivo and in vitro. To evaluate the mechanism of this inhibitory effect of ethanol, we investigated the role of nitric oxide (NO) on contractility of isolated LES and LEB circular muscle strips using inhibitors of NO synthase (NOS), NG-nitro-L-arginine methyl ester and NG-nitro-L-arginine. Ethanol significantly decreased LES basal tone. This effect was not mediated by NO, because inhibition was not prevented by inhibitors of NOS. Electrical field stimulation caused an On-response relaxation from LES strips, and an Off-response contraction from both LES and LEB strips. Inhibitors of NOS prevented the On-response relaxation of LES, but had no significant effect on LES Off-response contraction. Ethanol potentiated the On-response relaxation of the LES Off-response contraction. Ethanol potentiated the On-response relaxation of LES, but had no significant effect on Off-response contraction. Ethanol's potentiating effect of the On-response relaxation is NO-mediated, because it was abolished by NOS inhibitors. Ethanol also inhibited carbachol-induced LES contractility. This inhibitory affect was NO-mediated, because NOS inhibitors abolished it. Ethanol inhibited both the Off-response contraction and carbachol-induced contraction of LEB strips. These effects were not NO-mediated, because they were not affected by NOS inhibitor. These data suggest that NO is not a mediator for the inhibitory effect of ethanol on LEB contractility, and that NO seems to be a mediator of ethanol inhibition of some aspects of LES motor functions.

Animals↗
PubMed2000

Etiology, forms, and prognosis of gastrointestinal dysfunction resembling vagal indigestion occurring after surgical correction of right abomasal displacement.

The objectives of this study were to determine the etiology and types of vagal indigestion (VI) occurring after right displacement of the abomasum or abomasal volvulus (RDA/AV), and the prognosis for each type. Data of cows presented for RDA/AV from a retrospective (n = 288) and a prospective (n = 132) study were used. Vagal indigestion occurred in 39 and 22 cows in each study, respectively. A necropsy was performed in 29 cases. Gastric compartment dilation compatible with VI type III or IV occurred in 23 cases. An abnormal gastric wall was detected in 22 cases. Peritonitis was present in 18 cows. Vagal nerve lesions were present in 5 out of 13 cases studied. Clinical, hematological, and necropsy results suggested a classification of VI with respect to presence or absence of peritonitis. Gastric wall damage, peritonitis and vagal nerve lesions appear important in the etiology. Considering peritonitis occurrence, antimicrobial therapy appears necessary in the treatment of RDA/AV.

Abomasum↗
PubMed1975

Gastrointestinal dysfunction in immunoglobulin deficiency. Effect of corticosteroids and tetracycline.

Idiopathic late-onset immunoglobulin deficiency in a young man was associated with achlorhydria and a severe intestinal malabsorption syndrome that did not respond to conventional therapy. Combined therapy with high doses of prednisone and tetracycline hydrochloride resulted in weight gain, cessation of diarrhea, improved absorption of water, fat, and vitamin B12, and production of gastric acid after stimulation with histamine. Serum immunoglobulin levels, however, did not increase.

Achlorhydria↗